Regulation of autoreactive B cells in an anti-DNA antibody- knock-in mouse model
Regulation of autoreactive B cells in an anti-DNA antibody- knock-in mouse model
批准号:
23791111
负责人:
YOSHIFUJI Hajime
金额:
$2.58万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2011
资助国家:
日本
项目状态:
已结题
起止时间:
2011 至 2012
中文摘要
仅抑制自身反应性淋巴细胞的疗法对于系统性红斑狼疮(SLE)的治疗是期望的。我们分析了SLE模型“抗DNA抗体敲入小鼠”,以了解自身反应性B细胞是如何调节的。纯合子脾B细胞明显减少,骨髓中B细胞成熟受到抑制。人类的B细胞倾向于移动到脾脏的边缘区。人B细胞IgM/IgD表达水平较低,推测其受无反应性调节。进一步的分析将阐明SLE的病理生理学。
英文摘要
A therapy that inhibits only autoreactive lymphocytes is desirable for the treatment of systemic lupus erythematosus (SLE). We analyzed an SLE model ‘anti-DNA-antibody-knock-in mouse' to know how autoreactive B cells are regulated. The homozygotes' splenic B cells were significantly decreased, and their maturation was inhibited in the bone marrow. Homo's B cells tended to move to the marginal zone in their spleens. Homo's B cells showed low expression levels of IgM/IgD, and were supposed to be regulated by anergy. Further analyses will elucidate the pathophysiology of SLE.
期刊论文(0)
专著(0)
科研奖励(0)
会议论文
SLE モデルマウスにおける自己反応性 B 細胞制御メカニズム
SLE 模型小鼠自身反应性 B 细胞的调节机制
DOI:
--
发表时间:
2012
期刊:
リウマチ科
影响因子:
--
作者:
[Akiko Okamoto, Keishi Fujio, Kazuhiko Yamamoto, 吉藤 元.]
通讯作者:
吉藤 元.
SLEモデルマウスにおける自己反応性B細胞制御メカニズム
SLE模型小鼠自身反应性B细胞控制机制
DOI:
--
发表时间:
2011
期刊:
影响因子:
--
作者:
[Akiko Okamoto, Keishi Fujio, Kazuhiko Yamamoto, 吉藤 元., 吉藤 元]
通讯作者:
吉藤 元
海外基金